Occupational and Environmental Medicine
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The association between birth weight and exposure to benzene, work stress, and other occupational and environmental hazards was investigated.
In a large petrochemical industry, 792 pregnant workers were enrolled and followed up through delivery between May 1996 and December 1998. Exposure to benzene and other solvents was assessed by an industrial hygienist based on each woman's job title and workplace information. Other occupational and environmental exposures and personal information, including perceived work stress, exposure to noise, physical exertion at work, and passive smoking, were obtained by an interview questionnaire. Univariate and multivariate regression models were used to examine the individual and combined associations of occupational and environmental exposures with birth weight, with adjustment for major confounders including gestational age.
In the univariate model, birth weight was negatively associated with exposure to benzene (−58 g (95% confidence interval (95% CI), −115 to −2)) and with work stress (−84 g (95% CI, −158 to −10)). In the multivariate model, there was a significant interaction between exposure to benzene and work stress relative to reduced birth weight, after adjustment for other environmental and occupational exposures and personal variables. Adjusted mean birth weight was 3445 g (95% CI 3401 to 3489) among those with neither exposure, 3430 g for those with exposure to benzene only, 3426 g for those with work stress only, and 3262 g (95% CI 3156 to 3369) for those with both exposures. In other words, there was 183 g (95% CI 65 to 301) reduction in birth weight among those with both exposure to benzene and work stress compared with those with neither exposure. Other work or environmental factors could not explain these findings.
Low level exposure to benzene and work stress interact to reduce birth weight in this population.
To explore social inequalities in residential exposure to road traffic noise in an urban area.
Environmental injustice in road traffic noise exposure was investigated in Paris, France, using the RECORD Cohort Study (n=2130) and modelled noise data. Associations were assessed by estimating noise exposure within the local area around participants' residence, considering various socioeconomic variables defined at both individual and neighbourhood level, and comparing different regression models attempting or not to control for spatial autocorrelation in noise levels.
After individual-level adjustment, participants' noise exposure increased with neighbourhood educational level and dwelling value but also with proportion of non-French citizens, suggesting seemingly contradictory findings. However, when country of citizenship was defined according to its human development level, noise exposure in fact increased and decreased with the proportions of citizens from advantaged and disadvantaged countries, respectively. These findings were consistent with those reported for the other socioeconomic characteristics, suggesting higher road traffic noise exposure in advantaged neighbourhoods. Substantial collinearity between neighbourhood explanatory variables and spatial random effects caused identifiability problems that prevented successful control for spatial autocorrelation.
Contrary to previous literature, this study shows that people living in advantaged neighbourhoods were more exposed to road traffic noise in their residential environment than their deprived counterparts. This case study demonstrates the need to systematically perform sensitivity analyses with multiple socioeconomic characteristics to avoid incorrect inferences about an environmental injustice situation and the complexity of effectively controlling for spatial autocorrelation when fixed and random components of the model are correlated.
OBJECTIVES: Chloroplatinates are potent allergens but other soluble platinum compounds such as tetraammine platinum dichloride (TPC) do not provoke reactions in subjects who are sensitive to chloroplatinates. TPC has been used in the manufacture of autocatalysts for 20 years. This study analyses 20 year data on exposure to soluble platinum compounds and medical surveillance to confirm that TPC is not allergenic. METHODS: Workers in three distinct operations were exposed to soluble platinum compounds as chloroplatinates, chloroplatinates with TPC, or to TPC alone. Results of personal air sampling for soluble platinum compounds were compared together with the results of medical surveillance. RESULTS: The levels of exposure to soluble platinum compounds in each operation were comparable but the incidence of allergy was significantly different. In a subgroup of workers consistently exposed to chemical processes in each operation, the cumulative chance of being sensitised after 5 years of exposure was estimated as 51% for chloroplatinate exposure, 33% for mixed exposure, and 0% for TPC alone. The differences in sensitisation rates could not be explained by age, sex, and atopy. Nor could they be explained by the increased frequency of smoking in the workers with chloroplatinate exposure, despite the markedly higher risk of sensitisation in smokers. The differences could only be explained by the chemical stability of TPC. CONCLUSIONS: This study shows that the soluble platinum compound TPC is not allergenic under normal industrial conditions. Characterisation of the chemical compound (speciation) is essential to prevent stringent exposure limits being imposed for all soluble compounds on a generic basis.
To investigate changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation associated with changes in long-term exposure to ambient air pollutants.
We conducted secondary analyses of data on blood pressure and blood biochemistry markers from the Social Environment and Biomarkers of Aging Study in Taiwan and air pollution data from the Taiwan Environmental Protection Administration in 2000. Associations of 1-year averaged criteria air pollutants (particulate matter with aerodynamic diameters <10 μm (PM10) and <2.5 μm (PM2.5), ozone (O3), nitrogen dioxide (NO2), sulfur dioxide and carbon monoxide) with systolic blood pressure, diastolic blood pressure, total cholesterol, triglycerides, high-density lipoprotein cholesterol, fasting glucose, haemoglobin A1c (HbA1c), interleukin 6 (IL-6) and neutrophils were explored by applying generalised additive models.
After controlling for potential confounders, we observed that increased 1-year averaged particulate air pollutants (PM10and PM2.5) and NO2were associated with elevated blood pressure, total cholesterol, fasting glucose, HbA1c, IL-6 and neutrophils. Associations of increased 1-year averaged O3with elevated blood pressure, total cholesterol, fasting glucose, HbA1c and neutrophils were also observed. In particular, our two-pollutant models showed that PM2.5was more significantly associated with end-point variables than two gaseous pollutants, O3and NO2.
Changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation are associated with long-term exposure to ambient air pollutants. This might provide a link between air pollution and atherosclerotic cardiovascular diseases.
OBJECTIVES: To determine the association between maternal occupational exposure to anaesthetic gases and risk of spontaneous abortion. METHODS: A meta-analysis was performed of published epidemiological studies identified from literature reviews, unsystematic perusal of reference lists of relevant publications, and two Medline searches (1984-92, keywords: anaesthetic gases; anaesthetics; anaesthetics, local; operating rooms; operating room nursing; pregnancy; abortion; 1985-92, keywords: anaesthetics; adverse effects; occupational exposure; anaesthesia, inhalation; operating room nursing; pregnancy; abortion). All peer reviewed studies were retained. Student theses were excluded, as were conference abstracts, unpublished material, and two studies in which data on paternal and maternal occupational exposures were pooled. The relative risk of spontaneous abortion was estimated. RESULTS: One study found no increase in risk of abortion when gases were scavenged or when the exposure to unscavenged gases was low. None of the studies included ambient gas sampling. 24 comparisons between exposed and unexposed women, obtained from 19 reports, were included. The overall relative risk was 1.48 (95% confidence interval (95% CI), 1.4 to 1.58). To test whether this result was influenced by the quality of the studies, the validity of the reviewed papers was rated on the basis of three criteria: appropriateness of the unexposed comparison group, control for non-occupational confounding variables, and response rate. The estimate of risk increased to 1.9 (95% CI, 1.72 to 2.09) when analysis was restricted to the six comparisons which were rated the most rigorous. CONCLUSIONS: Epidemiological studies based on data obtained in the prescavenging era indicate an increased risk of spontaneous abortion. The estimated increased risk was not diminished but rather increased by exclusion of the more methodologically flawed studies.
The mortality of a census population and a prospective cohort of men employed on an antimony smelter in the north east of England was followed up from 1961-1992. The workers studied were exposed to a variety of agents including antimony and its oxides, arsenic and arsenic oxides, sulphur dioxide, and polycyclic aromatic hydrocarbons. The regional mortality rates were used to calculate expected deaths and a group of zircon sand workers employed on the site were used as a comparison group. For the census population of men working on the smelter before 1961 a significant increase in deaths from lung cancer was found (32 observed v 14.7 expected, P < 0.001). A similar excess was seen among maintenance men (12 observed v 5.3 expected P = 0.016). No such excess was found in the cohort recruited after 1960 (5 observed v 9.2 expected, maintenance workers 3 observed v 2.8 expected). There was evidence of a minimum latency period of around 20 years between first exposure and death from lung cancer. No evidence was found for a correlation between length of time worked and mortality from lung cancer. The results show that an increased risk of lung cancer existed in the workers employed before 1961, but it was not possible to attribute this excess to any particular agent. Mortality analysed by five year calendar periods of first exposure show a lessening of effect after 1955. Although the power of the study is clearly less for more recent periods of exposure the absence of any excess in the population after 1960 is encouraging.
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