Pascal Wild

Respiratory symptoms and bronchial responsiveness in lifeguards exposed to nitrogen trichloride in indoor swimming pools.

OBJECTIVES: To measure the levels of exposure to nitrogen trichloride (NCl3) in the atmosphere of indoor swimming pools and to examine how they relate to irritant and chronic respiratory symptoms, indices of pulmonary function, and bronchial hyperresponsiveness to methacholine in lifeguards working in the pools. METHOD: 334 lifeguards (256 men; 78 women) recruited from 46 public swimming pools (n = 228) and 17 leisure centre swimming pools (n = 106) were examined. Concentrations of NCl3 were measured with area samplers. Symptoms were assessed by questionnaire and methacholine bronchial challenge (MBC) test by an abbreviated method. Subjects were labelled MBC+ if forced expiratory volume in one second (FEV1) fell by > or = 20%. The linear dose-response slope was calculated as the percentage fall in FEV1 at the last dose divided by the total dose given. RESULTS: 1262 samples were taken in the 63 pools. Mean NCl3 concentrations were greater in leisure than in public pools. A significant concentration-response relation was found between irritant eye, nasal, and throat symptoms-but not chronic respiratory symptoms-and exposure concentrations. Among women, the prevalence of MBC+ was twice as great as in men. Overall, no relation was found between bronchial hyperresponsiveness and exposure. CONCLUSIONS: The data show that lifeguards exposed to NCl3 in indoor swimming pools are at risk of developing irritant eye, nasal, and throat symptoms. Exposure to NCl3 does not seem to carry the risk of developing permanent bronchial hyperresponsiveness, but this association might have been influenced by self selection. The possibility that subjects exposed to NCl3 are at risk of developing transient bronchial hyperresponsiveness cannot be confidently ruled out.

Shiftwork experience, age and cognitive performance

Changes of alertness and cognitive efficiency has been suggested in people whose circadian rhythms are disrupted, e.g. night or shift-workers. Data from field and laboratory studies have demonstrated short-term cognitive disturbances related to circadian rhythm disruption. By contrast, little is known about the long-term consequences of chronic sleep deprivation, as can be observed with shift-work, on cognitive abilities. The present paper is aimed at evaluating, on a large cross-sectional sample of workers, the long-term influence of shift-work on verbal memory and speed performances. Participants were 3237 workers aged 32, 42, 52, and 62 years of various occupational statuses included in the VISAT (Aging, Health and Work) cohort. Data collected by questionnaires included items on working hours and shift-work and sleep disorders. Cognitive abilities were assessed using neuropsychological tests. Current male shift-workers had lower cognitive performance than never exposed workers. In the same population, memory performance tended to decrease with increasing shift-work duration. Among former shift-workers, the cognitive performance of the participant having stopped shiftwork more than 4 years ago seemed to be increased, suggesting a possible reversibility of effects. In conclusion, this study demonstrated that cognitive functioning tends to be impaired by a long-term exposure to SW. As found by other authors, neuropsychological performance tends to decrease with the increases in the duration of exposure to SW.

Lung Cancer and Exposure to Metals: The Epidemiological Evidence

Exposure to metallic compounds is ubiquitous, with its widespread use in industry and its presence, mostly in trace amounts, in the environment. This paper reviews the epidemiologic evidence of the relation between lung cancer and exposure to metallic compounds by building on and updating the corresponding International Agency for Research on Cancer (IARC) assessments. Given that most of the well-identified human populations with given metal exposure are in occupational settings, this review is mostly based on results in occupational epidemiology. The epidemiological evidence is shortly reviewed for accepted carcinogens: chromium, nickel, beryllium, cadmium, arsenic, and silicon, highlighting what is still unclear. We then review in more detail metals for which the evidence is less clear: lead, titanium, iron, and cobalt. There is scarce evidence for the human carcinogenicity of titanium. Exposure to titanium dioxide is associated with lung cancer excesses in one large study, but this excess may be due to confounders. The evidence for lead is contradictory. The lung cancer risk is presented as a function of a post hoc exposure ranking but no dose-response relationship is found. A weak but consistent lung cancer excess in many populations exposed to iron oxides but it is not possible to state on causality. Finally the evidence in the hard metal industry is presented, which suggests a possible carcinogenic effect of cobalt in presence of tungsten carbide. A short discussion presents the limitations of epidemiology in assessing the carcinogenicity of metals.

trans,trans-Muconic acid, a reliable biological indicator for the detection of individual benzene exposure down to the ppm level

Summarytrans,trans-Muconic acid (2,4-hexadienedioic acid) (t,t-MA) is a minor benzene metabolite which can be used as a biological indicator for benzene exposure. The purpose of the study was to evaluate the limits of use of t,t-MA for detection and quantification of occupational exposures to benzene, particularly on an individual scale, phenol being used as the metabolite of reference. A simple and sensitve method previously described by the authors was carried out to analyse t,t-MA in 105 end-of-shift urinary samples from 23 workers exposed to benzene used as an extraction solvent for “concretes” recovery in the perfume industry. Good correlations were found between atmospheric benzene and both metabolites (uncorrected or corrected for creatinine) or between the metabolites themselves, with correlation coefficients from 0.81 to 0.91 (P < 0.0001). Correlation-coefficients were not improved after correction for creatinine. The overall individual benzene exposure range, median, and arithmetic mean were respectively 0.1–75, 4.5, and 9.0 ppm with corresponding t,t-MA excretion of 0.1–47.9, 5.2 and 8.9 mg/l (uncorrected) and phenol excretion of 1.4–298, 30.9, and 42.2 mg/l (uncorrected). In the control group (145 determinations for t,t-MA and 76 for phenol from 79 individuals) the range, median, and arithmetic mean were respectively < 0.04–0.66, 0.08, and 0.13 mg/l (uncorrected t,t-MA) and 1.5–42.0, 9.85 and 11.3 mg/l (uncorrected phenol). t,t-MA was far more specific than phenol and could be easily and practically used to estimate with a given probability the upper or lower corresponding benzene concentrations down to around the ppm level. Biological exposure indices for benzene exposure to 10, 5, or 1 ppm could be set at 10, 5, or 1 mg t,t-MA/l (uncorrected).

A mortality study among mild steel and stainless steel welders.

A mortality study was carried out in conjunction with the European mortality study among welders coordinated by the International Agency for Research on Cancer (IARC). The study was aimed at assessing risks for lung cancer in relation to exposure to asbestos, welding fumes containing chromium and nickel, and tobacco smoke. The study included a cohort of 2721 welders and an internal comparison group of 6683 manual workers employed in 13 factories in France. The mortality of the two cohorts was studied from 1975 to 1988 by the historical prospective method. Job histories of welders were traced including welding processes used, metals welded, and proportion of worktime spent in welding. Data on smoking habits were collected from medical records. The observed number of deaths were compared with those expected (standardised mortality ratio (SMR)) based on national rates with adjustments for age, sex, and calendar time. The smoking habits of 87% of the whole study population were known. The distribution of welders and controls according to smoking was not statistically different. The overall mortality was slightly higher for welders (SMR = 1.02, 95% confidence interval (95% CI) 0.89-1.18) than for controls (SMR = 0.91, 95% CI 0.84-0.99). For lung cancer, the SMR was 1.24 (95% CI 0.75-1.94) for welders, whereas the corresponding value was lower for controls (SMR = 0.94, 95% CI 0.68-1.26). The SMR for lung cancer was 1.59 among non-shipyard mild steel welders (95% CI 0.73-3.02). This contrasted with the results for all stainless steel welders (SMR = 0.92, 95% CI 0.19-2.69), and for stainless steel welders predominantly exposed to chromium VI (SMR = 1.03, 95% CI 0.12-3.71). Moreover, SMRs for lung cancer for mild steel welders tended to increase with duration of exposure and time since first exposure, leading to significant excesses for duration > or = 20 years and latency > or = 20 years. Such a pattern was not found for stainless steel welders.

Lung cancer mortality in a site producing hard metals

OBJECTIVES To study the mortality from lung cancer from exposures to hard metal dust at an industrial site producing hard metals—pseudoalloys of cobalt and tungsten carbide—and other metallurgical products many of which contain cobalt. METHODS A historical cohort was set up of all subjects who had worked for at least 3 months on the site since its opening date in the late 1940s. A full job history could be obtained for 95% of the subjects. The cohort was followed up from January 1968 to December 1992. The exposure was assessed by an industry specific job exposure matrix (JEM) characterising exposure to hard metal dust from 1 to 9 and other possibly carcinogenic exposures as present or absent. Smoking information was obtained by interview of former workers. Standard lifetable methods and Poisson regression were used for the statistical analysis of the data. RESULTS Mortality from all causes was close to the expected (standardised mortality ratio (SMR) 1.02, 399 deaths) whereas mortality from lung cancer was significantly increased among men (SMR 1.70; 46 deaths, 95% confidence interval (95% CI) 1.24 to 2.26). By workshop, lung cancer mortality was significantly higher than expected in hard metal production before sintering (SMR 2.42; nine deaths; 95%CI 1.10 to 4.59) and among maintenance workers (SMR 2.56; 11 deaths; 95%CI 1.28 to 4.59), whereas after sintering the SMR was lower (SMR 1.28; five deaths; 95%CI 0.41 to 2.98). The SMR for all exposures to hard metal dust at a level >1 in the JEM was in significant excess (SMR 2.02; 26 deaths; 95%CI 1.32 to 2.96). The risks increased with exposure scores, duration of exposure, and cumulative dose reaching significance for duration of exposure to hard metal dust before sintering, after adjustment for smoking and known or suspected carcinogens. CONCLUSION Excess mortality from lung cancer was found among hard metal production workers which cannot be attributed to smoking alone. This excess occurred mostly in subjects exposed to unsintered hard metal dust.

Mortality study among workers producing ferroalloys and stainless steel in France.

A mortality study was carried out among the workers of a plant that had produced ferrochromium and stainless steel, and was still producing stainless steel, in order to determine whether exposure to chromium compounds, to nickel compounds, and to polycyclic aromatic hydrocarbons (PAH) could result in a risk of lung cancer for the exposed workers. The cohort comprised 2269 men whose vital status were recorded between 1 January 1952 and 31 December 1982. The smoking habits of 67% of the cohort members were known from medical records. The observed numbers of deaths were compared with the expected ones based on national rates with adjustment for age, sex, and calendar time. A low mortality, achieving statistical significance, was found from all causes (observed = 137, standardised mortality ratio (SMR) = 0.82) and from benign respiratory diseases (observed = one, SMR = 0.15). With regard to mortality from lung cancer, a non-significant excess appeared in the whole cohort (observed = 12, SMR = 1.40). Among the exposed workers, however, a significant lung cancer excess was found (observed = 11, SMR = 2.04) that contrasted with a low SMR (0.32) in the non-exposed group. This excess is unlikely to be explained by smoking, as the tobacco consumption of these two groups was similar. No trend was observed for mortality from lung cancer either according to time since first exposure, or according to duration of exposure. A nested case-control study clearly suggested that this excess of deaths from lung cancer was attributable to former PAH exposures in the ferrochromium production workshops rather than to exposures in the stainless steel manufacturing areas.

Mortality from lung cancer and cardiovascular diseases among stainless-steel producing workers

The mortality pattern of workers involved in the production of stainless steel (SS) was studied from 1968 to 1984 in order to investigate a possible risk of lung cancer in relation to exposure to chromium compounds, polycyclic aromatic hydrocarbons, and silica. The role of heat exposure in mortality from cardiovascular diseases also was examined. The cohort was comprised of 4,227 workers. Complete individual job histories were provided by the company (UGINE SA). The smoking habits of 24 percent of the cohort members were known from the interview of workers still active during the data collection. The observed numbers of deaths were compared with the expected ones based on national rates with adjustment for age, sex, and calendar time (standardized mortality ratio, SMR). No significant excesses of lung cancer were observed among workers employed in the manufacture of ferroalloys (SMR=0.68) and in the melting and casting of SS (SMR=1.04), whereas a significant excess appeared among SS foundry workers (SMR=2.29). This excess was higher and remained significant among workers with more than 30 years since first employment in the foundry area (SMR=3.34). Among subjects exposed to heat, no excess was observed for all cardiovascular diseases or for ischemic heart diseases.

An epidemiological study of the respiratory health of workers in the European refractory ceramic fibre industry

OBJECTIVES To investigate possible relations between respiratory health and past airborne exposure to refractory ceramic fibres (RCFs) and respirable dust in workers at six European factories, studied previously in 1987. METHODS The target population comprised all current workers associated with RCF production, plus others who had participated in 1987 “leavers”. Information was collected on personal characteristics, chest radiographs, lung function, respiratory symptoms, smoking, and full occupational history. Regression analysis was used to study relations between indices of health of individual workers and of cumulative exposure to airborne dust and fibres, and likely past exposure to asbestos. RESULTS AND DISCUSSION 774 workers participated (90% of current workers, 37% of leavers). Profusion of small opacities in exposed workers (51% 0/1+; 8% 1/0+) was similar to that among an unexposed control group but higher than in new readings of the 1987 study films (11% 0/1+, 2% 1/0+). The large difference between 1987 and recent films may be, at least in part, a reading artefact associated with film appearance. Small opacities of International Labour Organisation (ILO) category 1/0+ were not associated with exposure. An association of borderline significance overall between 0/1+ opacities and exposure to respirable fibres was found for some exposure periods only, the time related pattern being biologically implausible. Pleural changes were related to age and exposure to asbestos, and findings were consistent with an effect of time since first exposure to RCFs. Among men, forced expired volume in 1 second (FEV1) and forced vital capacity (FVC) were inversely related to exposure to fibres, in current smokers only. FEV1/ FVC ratio and transfer factor (TLCO) were not related to exposures. The estimated restrictive effect was on average mild. Prevalence of respiratory symptoms was low. Chronic bronchitis and its associated symptoms (cough, phlegm) showed some association with recent exposure to respirable fibres. This could be due to an irritant effect of RCFs.

Symptoms, airway responsiveness, and exposure to dust in beech and oak wood workers

OBJECTIVES To investigate the relation between levels of cumulative exposure to wood dust and respiratory symptoms and the occurrence of bronchial hyperresponsiveness among beech and oak workers. METHODS 114 Male woodworkers from five furniture factories and 13 male unexposed controls were examined. The unexposed control group was supplemented by 200 male historical controls. Statistical analyses were performed excluding and including the historical controls. Dust concentration was measured by personal sampling methods. Cumulative exposure to dust was calculated for each woodworker by multiplying the duration of the work by the intensity of exposure (years.mg/m3). Bronchial hyperresponsiveness was assessed by the methacholine bronchial challenge test. Subjects were labelled methacholine bronchial challenge positive if forced expiratory volume in 1 second (FEV1) fell by ⩾20%. The linear dose-response slope was calculated as the last dose divided by the total dose given. RESULTS 443 Dust samples were collected. The median cumulative exposure to dust was 110 years.mg/m3 with lower and upper quartiles at 70 and 160 years.mg/m3 Overall, no declines in FEV1 and forced vital capacity (FVC) were found with increasing exposures. A dose-response relation was found between intensity of exposure on the one hand, and sore throat, increased prevalence of positive methacholine bronchial challenge tests, and steeper dose-response slope, on the other. CONCLUSION Exposure to oak and beech dust may lead to the development of sore throat and bronchial hyperresponsiveness.